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1 Physiology & Pharmacology, Oregon Health & Science University, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: brooksv{at}ohsu.edu.
Water deprivation is associated with increased excitatory amino acid (EAA) drive of the rostral ventrolateral medulla (RVLM), but the mechanism is unknown. This study tested the hypotheses that the increased EAA activity is mediated by decreased blood volume and/or increased osmolality. This was tested in urethane-anesthetized rats, first, by determining if bilateral microinjection of kynurenate (KYN; 2.7 nmol) into the RVLM decreases arterial pressure less in water-deprived rats after normalization of blood volume by iv infusion of isotonic saline or after normalization of plasma osmolality by iv infusion of 5% dextrose in water (5DW). Water deprived rats exhibited decreased plasma volume and elevated plasma osmolality, hematocrit and plasma sodium, chloride and protein levels (all P<0.05). KYN microinjection decreased arterial pressure by 24±2 mmHg (P<0.05; n=17). The depressor response was not altered following isotonic saline infusion, but, while still present (P<0.05), was reduced (P<0.05) to -13±2 mmHg soon after 5DW infusion. These data suggest that the high osmolality, but not low blood volume, contributes to the KYN depressor response. To further investigate the action of increased osmolality on EAA input to RVLM, water replete rats were also studied after hypertonic saline infusion. While KYN microinjection did not decrease pressure immediately following the infusion, a depressor response gradually developed over the next 3 hr. Lumbar sympathetic nerve activity also gradually increased to up to 167±19% of control (P<0.05) 3 hr after hypertonic saline infusion. In conclusion, acute and chronic increases in osmolality appear to increase EAA drive of the RVLM.
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